半面痉挛发病机制的实验研究

Study on Pathogenic Mechanism of Hemifacial Spasm

利用动物实验对半面痉挛发病机理进行探讨，以明确神经异常纤维间传递或／和异位兴奋的发生部位。采用后颅窝手术径路开放动物桥小脑角后，在面神经根部放置硅胚夹，造成面神经纤维脱髓鞘，术后三周对面神经及其核团进行电生理及病理检测。发现面神经脱髓鞘部位可成为纤维间传导的主要部位。同时面神经核团出现结构变化和兴奋性增强，并对逆行电刺激产生泛化。提出在半面痉挛中可能存在着跨神经元病变。

In 17 cats,areas of focal injury were induced in the facial nerve root near the brain stem by implantation of V-clamp and catgut suture. The electrophysiological examinations were made at 3 weeks after the surgery。When the mandibular branch of the facial nerve was electrically stimulated,a combined activity potential and a delayed activity could be recorded from the orbicular ocular branch of the facial nerve. The delayed activity disappeared after the motomucleu of the facial nerve was blocked with injection of 2% Lidocaine(1、5μl).These phenomena suggeste that the artifacial synapses have been foimed among the demyelinating facial nerve. The antidromic impluse of the mandibular branch of the faciaI nerve spread to adjacent fibers through the artifacial synapses in REZ of the facial nerve and causes the svnki nases and spasm. Delayed activity may be caused by neurons of the motomucleu. Experimental lesion was also examined histologically at 3 weeks following implantation. Injured nerve showed areas of demyelination and Waller's degeneration of adjacent axons.The Nissle sub- stances at the neurons of the motornucleu were dissolved and disappeared.